Hayashi, Shizu
Professor
Research Interests
Smoking is the major risk factor for chronic obstructive pulmonary disease but only 10 to 15% of smokers develop this disease. To determine whether latent adenovirus infections contribute to the pathogenesis of this disease the aim of Dr. Hayashi's research is to understand how the adenovirus E1A protein regulates host genes in lung cells to increase the production of inflammatory mediators. For this she analyzes human lung tissue, cultures of human lung epithelial cells, and an animal model of latent adenovirus infection.
Selected Publications
Keicho N, Higashimoto Y, Bondy GP, Elliott WM, Hogg JC, Hayashi S. 1999. Endotoxin-specific NF-kB activation in pulmonary epithelial cells harbouring adenovirus E1A. Am. J. Physiol. Lung Cell. Mol. Physiol. 277: L523-L532
Yamada K, Elliott WM, Hayashi S, Roberts C, Brattsand R, Hogg JC, Vitalis TZ. 2000. Allergen induced eosinophilic airway inflammation: The induction of steroid resistance by latent adenovirus infection. J. Allergy Clin.Immunol. 106:844-851
Meshi B, Vitalis T, Ionescu D, Elliott WM, Liu C, Wang X-D, Hayashi, S, Hogg JC. 2002. Emphysematous lung destruction by cigarette smoke: The effects of latent adenoviral infection on the lung inflammatory response. Am. J. Respir. Cell Mol. Biol. 26: 52-57.
Higashimoto Y, Elliott WM, Behzad AR, Sedgwick EG, Takei T, Hogg JC, Hayashi S. 2002. Inflammatory mediator mRNA expression by adenovirus E1A transfected bronchial epithelial cells. Am. J. Respir. Crit. Care Med. 166:200-207.
Fujii T, Hogg JC, Keicho N, Vincent R, van Eeden SF, Hayashi S. 2003. Adenoviral E1A modulates inflammatory mediator expression by lung epithelial cells exposed to PM10. Am. J. Physiol. Lung Cell. Mol. Physiol. 284: L290-L297.
Ogawa E, Elliott WM, Higashimoto Y, Hughes F, Eichholtz TJ, Hogg JC, Hayashi S. 2004. Latent adenoviral infection induces the production of growth factors relevant to airway remodeling in COPD. Am. J. Physiol. Lung Cell. Physiol. 286:L189-L197.